Dataset Information

Proteomic analysis of intracranial aneurysm

ABSTRACT: Intracranial aneurysm (IA) is a pathological dilation of the cerebral artery which has a potential to rupture leading to sub arachnoid haemorrhage (SAH). One third of the patients with aneurysmal SAH (aSAH) develop symptomatic narrowing of the blood vessels called cerebral vasospasm. The outcomes in the above clinical scenarios are variable and devastating. The study was designed to decipher the molecular mechanisms underlying the pathophysiology of intracranial aneurysm formation, its rupture and subsequent development of vasospasm at the proteomic level. The study was done in two phases – discovery phase and validation phase. We performed iTRAQ-based quantitative proteomic analysis of brain vessel tissue and serum samples in three subgroups of patients with IA and compared them with those of control group (subjects with no cerebrovascular disorder) during the discovery phase. In validation phase, dysregulated proteins of biological significance i.e. ORM1 as a biomarker for unruptured aneurysm and MMP9 as a biomarker for cerebral vasospasm were validated in larger cohort of patients.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Brain, Blood Serum

SUBMITTER: Hemant Bhagat

LAB HEAD: Hemant Bhagat

PROVIDER: PXD013442 | Pride | 2022-09-07

REPOSITORIES: Pride

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Publications

Intracranial Aneurysm Biomarker Candidates Identified by a Proteome-Wide Study.

Sharma Tanavi T Datta Keshava K KK Kumar Munish M Dey Gourav G Khan Aafaque Ahmad AA Mangalaparthi Kiran Kumar KK Saharan Poonam P Chinnapparaj Shobia S Aggarwal Ashish A Singla Navneet N Ghosh Sujata S Rawat Amit A Dhandapani Sivashanmugam S Salunke Pravin P Chhabra Rajesh R Singh Dalbir D Takkar Aastha A Gupta Sunil K SK Prasad Thottethodi Subrahmanya Keshava TSK Gowda Harsha H Mukherjee Kanchan K KK Pandey Akhilesh A Bhagat Hemant H

Omics : a journal of integrative biology 20200611 8

The scientific basis of intracranial aneurysm (IA) formation, its rupture and further development of cerebral vasospasm is incompletely understood. Aberrant protein expression may drive structural alterations of vasculature found in IA. Deciphering the molecular mechanisms underlying these events will lead to identification of early detection biomarkers and in turn, improved treatment outcomes. To unravel differential protein expression in three clinical subgroups of IA patients: (1) unruptured ...[more]

PMID: 32525733

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Project description:BACKGROUND: Subarachnoid hemorrhage (SAH) is a devastating cerebrovascular disease with a poor prognosis. Accumulating studies have reported that gut microbiota contributes to the pathophysiology of several central nervous system diseases. However, whether SAH can change gut microbiota composition and affected gut microbiota is involved in the development of secondary brain injury following SAH remains unclear.METHODS: A retrospective case-control study was performed in unruptured intracranial aneurysm (UIA, CTL) and ruptured intracranial aneurysm (SAH) patients. Patients' fecal and serum samples were collected and sequenced by metagenome and metabolome. The experimental SAH mice models were established, and their feces and serum were also analyzed by 16S rRNA and metabolic sequencing. Fecal microbiota from SAH patients and mice was transplanted to ABX mice to investigate the relationship between the gut microbiota and secondary brain injury following SAH.RESULTS: SAH seriously influenced gut microbiota composition and significantly increased the relative abundance of the genus Escherichia. SAH also considerably reduced the production of gut microbiota-derived butyric acid. Furthermore, SAH-induced gut microbiota dysbiosis aggravated brain injury and cognitive deficits in ABX mice by promoting inflammatory response. Sodium butyrate (NaB) administration protected against secondary brain injury following SAH by inhibiting pyroptosis-related neuroinflammation, which is mediated by NLRP1/Caspase-1/GSDMD and Caspase-3/GSDME signaling pathways. NaB drinking pretreatment also alleviated secondary brain injury following SAH by increasing the relative abundance of butyric acid-producing bacteria, such as Dubosiella and Faecalibaculum, and decreasing the Escherichia abundance.CONCLUSION: SAH contributed to gut microbiota dysbiosis and changed gut microbiota exacerbated secondary brain injury after SAH. Supplement with gut microbiota-derived butyric acid protected against brain injury following SAH by inhibiting NLRP1/Caspase-1/GSDMD and Caspase-3/GSDME-mediated neuronal pyroptosis. Linked studies:UPLC-MS/MS assays of murine samples are reported in this study.UPLC-MS/MS assays of human samples are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS9087' rel='noopener noreferrer' target='_blank'>MTBLS9087</a>.

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	IA_serum_1_R1.raw	Raw
	IA_serum_1_R2.raw	Raw
	IA_serum_1_R3.raw	Raw
	IA_serum_2_R1.raw	Raw
	IA_serum_2_R2.raw	Raw